The acute coronary syndrome (ACS) is characterized by a spectrum of arterial diseases that include unstable angina and myocardial infarction. In the last 10 years, ACS has become the cause of up to 29% of deaths in the industrialized countries, becoming the main cause of death, and it will most probably stay that way for the year 2020. The physiopathogenesis of ACS include oxidative, inflammatory, and thrombotic processes. Diverse molecules participate in the processes, increasing of decreasing the damage. The genes that encode these molecules have been associated with the disease. However, in some cases inconsistent results in different populations have been reported. In this review the physiopathogenesis and the role of several candidate genes involved in the pathogenesis of ACS are discussed.